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Biomedical subjects

T Bergström

Publications and source records attributed to T Bergström.

At least 73 records · Page 4Linked to original sources
PubMed1993

Failure to demonstrate enterovirus aetiology in Swedish patients with dilated cardiomyopathy.

Attempts were made to establish a possible relationship between enterovirus infection and dilated cardiomyopathy (DCM) by use of serology, virus isolation from faecal samples, and detection of enteroviral RNA in endomyocardial biopsies (EMB) by the polymerase chain reaction (PCR). Sera from 63 patients with DCM and matched controls were examined for enterovirus infection by mu-capture IgM and indirect IgG ELISA. Thirty-six patients were further tested for the presence of enterovirus group-specific antigen (VP1) in an immunoassay system. The results were consistently negative. Faecal samples from 35 of these patients were negative by enterovirus isolation both when samples were cultured directly and after acid treatment. EMB from 35 patients were examined for enteroviral RNA by PCR; none of the samples was reactive. In conclusion, the results fail to indicate involvement of enteroviruses in the aetiology of DCM.

Antigens, Viral↗
PubMed1993

Viral infections trigger multiple sclerosis relapses: a prospective seroepidemiological study.

A neurological surveillance was combined with prospective recording of upper respiratory and gastrointestinal infections and serological diagnosis of five common viral infections in 60 benign multiple sclerosis patients, with a mean follow-up of 31 months. During 4-week at risk (AR) periods encompassing common infections, a significant excess of MS relapses was found in the AR period, with a relative risk of 1.3. A seasonal variation of the MS relapse rate was found with a minimum in summer. There was a significant correlation between the number of AR relapses and the number of common infections per month explaining the periannual distribution of relapses. The non-AR relapses showed no seasonal variation. There was a significant correlation between adenovirus CF titre rises associated with upper respiratory infections and the occurrence of a major MS relapse in the AR period (n = 7), while influenza infections were not followed by a major MS relapse (n = 6). Linear homologies have been demonstrated between adenovirus and basic myelin protein. The epidemiological approach is essential to our understanding of systemic antigens triggering multiple sclerosis activity.

Adult↗
PubMed1993

Recrudescence of herpes simplex virus type 1 in latently infected rats after trauma to oral tissues.

Tooth extraction in rats was used to trigger a latent HSV-1 infection. HSV-1 was inoculated unilaterally in the rat palates. Eight weeks later two molars were removed bilaterally. The trigeminal ganglia were co-cultivated and HSV-1 was isolated from 63% of the ganglia on the infected sides but from only 11% on control sides. The immune response pattern was analysed by immunoblotting of rat serum, and strong reactivity to HSV-1 specific cell polypeptides and glycoproteins (ICP6, gC, pgC, gD) was seen after reactivation. The extraction sockets were histopathologically evaluated and showed healing on the infected side in 26% compared to 63% in contralateral control sockets. The effect of acyclovir (ACV) treatment was elucidated and was found to influence the subsequent development of antibodies and to promote healing of the sockets. Vesiculation in intra- and subepithelial tissue was present on the infected side in 58% but in only 12% of ACV-treated animals. The present study in rats has shown that a latent HSV-1 infection can be established and reactivated by tooth extraction. Reactivation resulted in delayed healing of sockets on the latently infected side but not on the contralateral control side. HSV-1 reactivation was demonstrated serologically by immunoblotting. Healing was significantly promoted by administration of ACV, which also supports the contention that HSV-1 interferes with the healing process.

Acyclovir↗
PubMed1993

Herpes simplex virus type 1-induced hemagglutination: glycoprotein C mediates virus binding to erythrocyte surface heparan sulfate.

We recently reported that herpes simplex virus type 1 (HSV-1) can cause agglutination of murine erythrocytes (E. Trybala, Z. Larski, and J. Wisniewski, Arch. Virol. 113:89-94, 1990). We now demonstrate that the mechanism of this hemagglutination is glycoprotein C-mediated binding of virus to heparan sulfate moieties at the surface of erythrocytes. Hemagglutination was found to be a common property of all gC-expressing laboratory strains and clinical isolates of HSV-1 tested. Mutants of HSV-1 deficient in glycoprotein C caused no specific hemagglutination, whereas their derivatives transfected with a functional gC-1 gene, thus reconstituting gC expression, regained full hemagglutinating activity. Hemagglutination activity was inhibited by antibodies against gC-1 but not by antibodies with specificity for glycoproteins gB, gD, or gE or by murine antiserum raised against the MP strain of HSV-1, which is gC deficient. Finally, purified gC-1 protein, like whole HSV-1 virions, showed high hemagglutinating activity which was inhibited by heparan sulfate and/or heparin and was completely prevented by pretreatment of erythrocytes with heparitinase, providing evidence that gC-1 mediates hemagglutination by binding to heparan sulfate at the cell surface. Thus, HSV-1-induced hemagglutination is gC-1 dependent and resembles the recently proposed mechanism by which HSV-1 attaches to surface heparans on susceptible cells, providing a simple model for initial events in the virus-cell interaction.

Animals↗
PubMed1992

Cerebrospinal fluid anti-cerebellar soluble lectin antibodies in human immunodeficiency virus type 1 infection.

Cerebrospinal fluid samples from 14 human immunodeficiency type 1 (HIV-1) seropositive patients in various stages of HIV infection were tested for the presence of autoantibodies to an endogenous manose-binding protein, the cerebellar soluble lectin (CSL), which has recently been found to be detected in a high proportion of patients with multiple sclerosis. An immunoblotting test was used with rat CSL as antigen. Seven patients were positive for anti-CSL and seven were negative. The seven anti-CSL-positive patients had signs of intrathecal immunoglobulin G production measured as an elevated IgG index, while the seven anti-CSL-negative patients had a normal IgG index. There was no apparent relation between infectious stage and the presence of anti-CSL. Immunological reactions such as anti-CSL autoantibodies may be a similar pathogenic mechanism in HIV and multiple sclerosis brain disease.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Mapping neuroinvasiveness of the herpes simplex virus type 1 encephalitis-inducing strain 2762 by the use of monoclonal antibodies.

Monoclonal antibodies (MAbs) directed against herpes simplex virus (HSV)-coded glycoproteins gB, gC, gD and gE were employed in a an in vitro model of neuroinvasiveness using sensory neurons from rat dorsal root ganglion (DRG) cells. The neurons were cultured in at two-chamber system allowing infection via the neuritic extensions exclusively. The effects of 30 MAbs on viral replication of the encephalitis-derived HSV-1 strain 2762 and its less neuroinvasive variant 2762p11 were assayed in this model. One MAb reactive with gD gave a nine-fold reduction of the virus yields of both strains. One MAb directed against gB gave an enhanced virus yield of strain 2762, but not of the 2762p11 variant. Another gB-reactive MAb decreased the virus yield of strain 2762p11, but not of 2762 after neuritic infection. The findings indicate that an alteration of gB has occurred during the passage of the strain 2762. Mutants of the same strain were derived by infecting hybridomas producing MAb reactive with gB, gC, gD and gE, respectively. The gB hybridoma mutant showed a significantly lower neuroinvasiveness in the DRG model, and was non-virulent after snout infection of mice. We suggest that the structure of gB of the strain 2762 is of importance for the neuroinvasiveness of this strain.

Animals↗
PubMed1991

Discrimination of herpes simplex virus types 1 and 2 cerebral infections in a rat model.

A rat model was used to evaluate intertypic differences after intracranial (i.c.) inoculation of herpes simplex virus (HSV) types 1 and 2 strains with regard to neurovirulence and neuropathology, and influence of age on susceptibility. In adult rats, HSV-1 strains were more virulent than HSV-2 strains. HSV-1 replicated to higher titers in the central nervous system (CNS) of rats, as compared with HSV-2. In rats of less than 2-3 weeks of age, HSV-1 and HSV-2 were equally virulent, but morphological examination of rat brains showed type-specific differences in pathology and viral distribution already at the early postnatal stage. After HSV-1 infection, neuronal infection of the hippocampus, followed by cortical infection and edematous destruction dominated, while a preponderance of meningitis and invasive encephalitis was seen after HSV-2 infection. We suggest that the rat might be a useful model for human HSV infection in the CNS with discrimination between HSV-1 and HSV-2 infections, also at the early postnatal stage.

Aging↗
PubMed1990

Neurovirulence of herpes simplex virus types 1 and 2 isolates in diseases of the central nervous system.

Herpes simplex virus (HSV) isolates derived from the central nervous system of ten patients with HSV-1-induced encephalitis, one patient with multiple sclerosis, and 14 patients with HSV-2-induced meningitis were investigated for neurovirulence by assaying the LD50 after nose and intracerebral (i.c.) inoculation of mice. HSV-1 encephalitis strains were significantly more virulent after nose inoculation (i.e. neuroinvasive) when compared with HSV-1 isolates from patients with oral lesions only, whereas HSV-2 meningitis strains were significantly more virulent after i.c. inoculation when compared with HSV-2 isolates from patients with genital lesions only. No correlation between high neurovirulence (defined as low LD50 for both routes of infection) and replication in cell cultures of neuronal and non-neuronal cell lines was found, but the weakly neurovirulent HSV-1 strain isolated from a patient with multiple sclerosis gave low replication yields. After nose inoculation, a highly neuroinvasive HSV-1 laboratory reference strain replicated to high titers in nose tissue, the trigeminal ganglia and brainstem, while a strain with low neuroinvasiveness but high i.c. virulence replicated less well in the brainstem. Neuroinvasiveness of the virus strain might be one factor of relevance in the pathogenesis of HSV-1 encephalitis in man.

Animals↗
PubMed1990

Primary and recurrent herpes simplex virus type 2-induced meningitis.

In 27 patients with a first episode of herpes simplex virus type 2 (HSV-2)-induced meningitis, confirmed by virus isolation from the cerebrospinal fluid (CSF) or seroconversion to HSV-2, initial neurologic complications were found in 10 (37%) but subsided before 6 months in all patients. Long-term complications were recurrent meningitis in 5 (19%) and periodic headache related to genital HSV recrudescences in 4 (15%). Seven additional patients had possible HSV-2-induced recurrent meningitis. In contrast to the first episode of meningitis, virus isolation, HSV antigen detection, and IgG analyses in consecutive serum samples were of no diagnostic value in episodes of HSV-2-induced recurrent meningitis. Instead, immunoblotting was used to assay intrathecally produced IgG antibodies to the HSV-2 type-specific protein gG-2 in recurrent meningitis, when CSF was collected at a minimum of 3 days after onset.

Antibodies, Viral↗
PubMed1990

Neuroinvasion by herpes simplex virus. An in vitro model for characterization of neurovirulent strains.

A cell culture technique with rat dorsal root ganglion neurons cultured in a two-chamber system allowing exposure of neuritic extensions or neuronal cell soma to herpes simplex virus (HSV) infection was exploited for studies of viral neuroinvasiveness. Four groups of HSV strains were investigated. Type 1 strains were isolated from cases of either encephalitis or mucocutaneous infections and type 2 strains were from cases of meningitis or genital infections. The neuroinvasiveness of the type 1 encephalitis strains was significantly greater than the neuroinvasiveness calculated for the type 1 strains of cutaneous origin or for either of the type 2 strains. From our evaluation of the rates of neuritic uptake and axonal transport and the rate of replication in dorsal root ganglion cells and skin fibroblasts, we concluded that the differences observed in neuroinvasiveness probably reflected differences in early virus-nerve cell interactions, i.e. virus attachment and fusion with the neuritic plasma membrane.

Animals↗
PubMed1990

Treatment of primary and recurrent herpes simplex virus type 2 induced meningitis with acyclovir.

We describe therapy with acyclovir in 1 patient with acute meningitis induced by herpes simplex virus type 2 (HSV-2) and in 1 patient with ascending myelitis in connection with meningitis after a primary genital HSV-2 infection. In addition, intermittent or continuous acyclovir prophylaxis against meningitis was employed in 3 patients with recurrent meningitis of probable HSV-2 etiology. Possible beneficial effects of the treatment were seen.

Acyclovir↗
PubMed1990

Mercury exposure of different origins among dentists and dental nurses.

Mercury exposure was studied among dental personnel with the use of urinary mercury excretion rates and questionnaires. The study covered 314 dentists and dental nurses employed in public clinics and private practices in Stockholm. The obtained urinary mercury excretion rates were analyzed by stepwise regression for assigning them to different origins, such as environmental factors, number of amalgam surfaces, chewing of gum, kind of employment and profession, age, sex, amalgam handling time, and use of amalgam capsules. On the average the occupational contribution to the total urinary mercury excretion rate was small and of the same order as the contribution from their own amalgam fillings (approximately 2 micrograms of mercury/24 h). There were, however, individuals showing excretion rates close to the levels at which effects on the central nervous system and the kidneys have been reported.

Adult↗
PubMed1989

[Is Mollaret's meningitis caused by herpes simplex virus type 2?].

Mollaret's meningitis is characterised by recurrent, brief episodes of serous meningitis with symptom-free intervals. Although viral etiology has been suspected, no pathogenic agent has hitherto been found. Using the immunoblot technique, we found IgG antibodies of intrathecal origin against the HSV-2-specific protein, gG2, in a patient with Mollaret's meningitis. Since being put on prophylactic acyclovir treatment twelve months ago, the patient has had no further episodes of meningitis. Because of the similarities between Mollaret's meningitis, recurrent HSV-2 meningitis, and the findings in the case reported here, HSV-2 is suggested as a possible cause of Mollaret's meningitis in general.

Adult↗
PubMed1989

Isolation of herpes simplex virus type 1 during first attack of multiple sclerosis.

Herpes simplex virus type 1 was isolated from the cerebrospinal fluid of a patient during the first attack of multiple sclerosis. This is the first virus to be isolated from the central nervous system of a living patient with MS. The virus was identified as herpes simplex virus type 1 by restriction endonuclease analysis and by an enzyme immunoassay using monoclonal antibodies. Antibodies against type 1 but not type 2 were detected in consecutive samples of serum and cerebrospinal fluid. The patient has since entered a progressive phase of multiple sclerosis. The isolated type 1 strain might be of pathogenetic relevance to the development of multiple sclerosis in this patient.

Antibodies, Monoclonal↗